This article presents information on the types of carcinogens that one may be exposed to through their occupation. The ‘National Agency for Research on Cancer’ (IARC) has classified more than sixty disease causing carcinogens and there are at least 10,000 cases of cancer in males each year.

 The cancer which is most strongly linked to occupational disease is: mesothelioma; accounting for 80-90% of occupational cancer in men exposed to asbestos.

The second most strongly related occupational disease is: cancer of the nasal cavity and sinuses which accounts for approximately 34% of  occupational disease.

And thirdly - lung cancer accounts for approximately 17% of deaths in males and up to 5% in females exposed to occupational carcinogenic. The most predominant substances that cause occupation-related lung cancer are: metals, arsenic, radon, asbestos, and  Polycyclic Aromatic Hydrocarbons. 

The following list represents the types of occupational carcinogens, type of occupation, and related risk of cancer.

Aromatic Amines

Manufactured in dyes and pigments such as:

• Ÿ         Plastics
• Ÿ         Textiles
• Ÿ         Paints
• Ÿ         Paper
• Ÿ         Drugs & Pesticides
• Ÿ         Antioxidants - (rubber tyres and cable preparation)

Related Carcinogenic Risk  - Bladder Cancer.

Arsenic

• Ÿ         Mining -  (copper, Smelting)
• Ÿ         Vineyard workers - ‘Pesticide Production’ - (arsenical pesticides)

Related Carcinogenic Risk - Lung Cancer

Asbestos

• Ÿ         Shipbuilding - (construction)  ‘
• Ÿ         Milling, and Mining
• Ÿ         By-Product Manufacturing - Sheet Metal Workers, Insulating, and Cement Industry
• Ÿ         Plumbing
• Ÿ         Carpentry

Related Carcinogenic Risk   - Mesothelioma , Asbestosis.

Benzene

• Ÿ         Solvents - (used in the production of shoes)
• Ÿ         Chemical Pharmaceutical
• Ÿ         Rubber Industry
• Ÿ         Printing Industry
• Ÿ         Gasoline Additive.

Related Carcinogenic Risk - Leukaemia.

Diesel

• Ÿ         Transportation Industry (workers/drivers)
• Ÿ         Bus Drivers
• Ÿ         Road Maintenance workers
• Ÿ         Mechanics
• Ÿ         Dock Workers.

Related Carcinogenic Risk  - Lung Cancer.

Formaldehyde

• Ÿ         Production
• Ÿ         Pathologists
• Ÿ         Medical Pathology Technicians
• Ÿ         Plastics
• Ÿ         Textiles
• Ÿ         Plywood Industry

Related Carcinogenic Risk - Nasopharynx (cancer of the nasal part of the pharynx)

Leather Dust

Boot and Shoe Manufacture Workers and Repairers

Related Carcinogenic Risk - Cancer of the Lung, Sinuses, and Nasal Cavity.

Certain Metal compounds

Metals such as: Cadmium, Chromium IV, Nickel Sulphides, Oxides, Beryllium.

• Ÿ         Iron and Steel foundry
• Ÿ         Metal Founding and Welding
• Ÿ         Manufacturing of Cadmium Oxide
• Ÿ         Cadmium Alloys and Pigments
• Ÿ         Nickel -Cadmium Production
• Ÿ         Chromate Production
• Ÿ         Iron and Metal ware Workers
• Ÿ         Mechanics

Related Carcinogenic Risk - Skin Cancer

Mineral Oils

• Ÿ         Metal Workers
• Ÿ         Printing Industry

Related Carcinogenic Risk  - Lung Cancer.

Polycyclic Aromatic Hydrocarbons 

Industries with Exposure to Soot and Coal Tar such as:

• Ÿ         Paving and Roofing
• Ÿ         Smelting and Metal Founders
• Ÿ         Engine and Motor Exhausts
• Ÿ         Chimney Sweeps
• Ÿ         Coal Gasification

Related Carcinogenic Risk - Lung, Bladder, and Skin Cancer.

Radon

 Workers in Underground Haematite Mines

Related Carcinogenic Risk  - Lung Cancer.

Silica

• Ÿ         Mining
• Ÿ         Stone Quarrying
• Ÿ         Granite Production
• Ÿ         Ceramic and  Pottery Industries
• Ÿ         Steel Production

Related Carcinogenic Risk - Lung Cancer.

UV Radiation

Outdoor occupations

Related Carcinogenic Risk  - Skin Cancer.

Wood Dust

• Ÿ         Furniture and Cabinet Making
• Ÿ         Logging and Sawmill Workers
• Ÿ         Pulp and Paperboard Industry

Related Carcinogenic Risk - Cancer of Sinuses and Naval Cavities.

Vinyl Chloride

• Ÿ         Production of Polyvinyl and Vinyl Chloride
• Ÿ         Plastics, Rubber, and Resins
• Ÿ         Car Interior Workers
• Ÿ         Furniture Makers
• Ÿ         Transportation Workers

 

Related Carcinogenic Risk  - Liver Cancer.

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]]> http://www.mesotheliomalungs.org/occupational-cancer-causing-hazards/feed 2 http://www.mesotheliomalungs.org/occupational-lung-disease http://www.mesotheliomalungs.org/occupational-lung-disease#comments Fri, 05 Jun 2009 16:36:59 +0000 Ann-Marie Waters http://www.mesotheliomalungs.org/occupational-lung-disease Exposure to dusts, gases, vapours and fumes at work can lead to the development of the following types of lung disease.
• Acute bronchitis and even pulmonary oedema from irritants such as sulphur dioxide, chlorine, ammonia, or the oxides of nitrogen.
• Pulmonary fibrosis due to mineral dust.
• Occupational asthma, this is now the commonest industrial lung disease in the developed world.
• Extrinsic allergic alveoli
• Bronchial carcinoma due to industrial agents (e.g. asbestos, polycyclic hydrocarbons, radon in mines).

The degree of fibrosis that follows inhalation of mineral dust varies. While iron (siderosis), barium (baritosis) and tin (stannosis) lead to dramatic dense nodular shadowing on the chest X-ray, their effect on lung function and symptoms is minimal. Exposure to silica or asbestos, on the other hand, leads to extensive fibrosis and disability. Coal dust has an intermediate fibrogenic effect and accounts for 90 percent of all compensated industrial lung diseases in the UK. The term ‘pneumoconiosis’ means the accumulation of dust in the lungs and the reaction of the tissue to its presence. The term is not wide enough to encompass all occupational lung disease and is now generally used only in relation to coal cost and its effect on the lung.

 

Coal-worker’s pneumoconiosis

 



 

 

 

 

 

 

 

Improved conditions and the progressive contraction of the coal industry in the UK have led to a considerable reduction in the number of cases of pneumoconiosis. The disease is caused by dust particles approximately 2-5um in diameter that are retained in the small air-ways and alveoli of the lung. The incidence of the disease is related to total dust exposure, which is highest at the coal face, particularly if ventilation and dust suppression are poor. Two very different syndromes result from the inhalation of coal.

Simple pneumoconiosis

This simply reflects the deposition of coal dust in the lung. It produces fine micro nodular shadowing on the chest X-ray and is by far the most common type of pneumoconiosis. It is graded on the chest X-ray appearance according to standard categories set by the ‘International Labour Office’. Considerable dispute remains about the effects of simple pneumoconiosis on respiratory function and symptoms. In many cases the symptoms are due to ‘Chronic Obstructive Pulmonary disease’, (COPD) related to cigarette smoking, but this is not always the case. Recent change to UK workers compensation legislation means that coal miners who develop (COPD) may be compensated for their disability regardless of their chest X-ray appearance.

Categories of simple pneumoconiosis are as follows:

• Small round opacities definitely present but few in number
• Small round opacities numerous but normal lung markings still visible
• Small round opacities very numerous and normal lung markings partly or totally obscured

The importance of simple pneumoconiosis is that it may lead to the development of ‘Progressive Massive Fibrosis – commonly known as (PMF). PMF virtually never occurs on a background of category 1 simple pneumoconiosis but occurs in about 7 percent of those with category 2 simple pneumoconiosis and in 30 percent of those with category 3. Miners with category 1 pneumoconiosis are unlikely to receive compensation unless they also have evidence of (COPD). Those with more extensive radiographic changes may be compensated solely on the basic of their X-ray appearances.

 

Progressive massive fibrosis

 



 

 

 

 

 

 

In PMF, patients develop round fibrotic masses several centimetres in diameter, almost invariably in the upper lobes and sometimes having necrotic central cavities. The pathogenesis of PMF is still not understood, though it seems clear that some fibrogenic promoting factor is present in individuals developing the disease. At one time this was thought to be M. Tuberculosis, but it is more probably due to immune complexes, analogous to the development of large fibrotic nodules in coal miners with rheumatoid arthritis (Caplan’s syndrome).

Both rheumatoid factor and antinuclear antibodies are often present in the serum of patients with PMF. Also, pathologically there is apical destruction and disruption of the lung, resulting in emphysema and airway damage. Lung function tests show a mixed restrictive and obstructive ventilatory defect with loss of lung volume, irreversible airflow limitation and reduced gas transfer. The patient with PMF suffers considerable effort dyspnoea, usually with a cough. The sputum can be black. The disease can progress (or even develop) after exposure to coal dust has ceased and may lead to respiratory failure.

 

Silicosis

 



 

 

 

 

 

 

 

 

This disease is uncommon, though it may still be encountered in workers foundries where sand used in moulds has to be removed from the metal casts (fettling), in sand blasting, and amongst stonemasons, pottery and ceramic workers. Silicosis is caused by the inhalation of silica (silicon dioxide). This dust is highly fibrogenic. For example, a coal miner can remain healthy with 30g of coal dust in his lungs but 3g of silica is sufficient to kill. Silica seems particularly toxic to alveolar macrophages and readily initiates fibro genesis. The chest X-ray appearances and clinical features of silicosis are similar to those of PMF, but distinctive thin streaks of calcification may be seen around the hilar lymph nodes (eggshell’ calcification).

 

Asbestosis

 



 

 

 

 

 

 

 

 

 

Asbestos is a mixture of silicates of iron, magnesium, nickel, cadmium and aluminium, and has the unique property of occurring naturally as a fibre. It is remarkably resistant to heat, acid and alkali, and has been widely used for roofing, insulation and fireproofing. Asbestos has been mined in southern Africa, Canada, and Eastern Europe. Several different types of asbestos are recognised: about 90 percent of asbestos is chrysotile, 6 percent crocidolite, and 4 percent amosite. Chrysotile or white asbestos is the softest asbestos fibre.

Each fibre is often as long as 2cm but only a few microns thick. It is less fibrogenic than crocidolite. Crocidolite (blue asbestos) is particularly resistant to chemical destruction and exists in straight fibres up to 50mm in length and 1-2um in width. Crocidolite is the most likely type of asbestos to produce asbestosis and mesothelioma. This may be due to the fact that it is readily trapped in the lung. Its long, thin shape means that it can be inhaled, but subsequent rotation against the long axis of the smaller airways, particularly in turbulent airflow during expiration, causes the fibres to impact.

Crocidolite is also particularly resistant to macrophages and neutrophil and enzymatic destruction. Exposure to asbestos occured particularly in ship building yards and in power stations, but its ubiquitous use meant that low levels of exposure were common.

Up to 50 percent of urban dwellers have been found to have evidence of asbestos bodies (asbestos fibre covered in protein secretions) in their lungs at post-mortem. Regulations in the UK prevent the use of crocidolite and severely restrict the use of chrysotile. Careful dust control measures are enforced, which should eventually abolish the problem.

Workers continue to be exposed to blue asbestos in the course of demolition or in the replacement of insulation, and it should be remembered that there is a considerable time lag between exposure and development of the disease, particularly mesothelioma (20-40 years).

A synergistic relationship between asbestos and cigarette smoking and the development of bronchial carcinoma, usually Adenocarcinoma, exists; the risk is multiplied fivefold above the risk attributable to smoking. The risk of lung cancer is also increased in non-smokers, especially in those who have parenchyma asbestosis but also in those who pleural plaques without parenchyma fibrosis.

Bilateral diffuse pleural thickening, asbestosis, mesothelioma and asbestos-related carcinoma of the bronchus are all eligible for industrial injuries benefit in the UK, but account for only one-quarter of the number of cases of compensation compared with coal-worker’s pneumoconiosis.

Asbestosis is defined as fibrosis of the lungs caused by asbestos dust, which may or may not be associated with fibrosis of the parietal or visceral layers of the pleura. It is a progressive disease characterized by the breathlessness and accompanied by finger clubbing and bilateral basal end-inspiratory crackles. Fibrosis, not detectable on chest X-ray, may be revealed on CT scan. No treatment is known to alter the progress of the disease, though corticosteroids are often prescribed.

The number of cases of mesothelioma has increased progressively since the mid-1980s and has now reached over 1000 cases per year. Pleural effusions are the most common. I.e. persistant chest wall pain, which should raise the index of suspicion even if the initial pleural fluid or biopsy samples are non-diagnostic. Often thoracoscopic biopsy is needed to obtain sufficient tissue for diagnosis. In the event of a positive pleural biopsy diagnosis, local radio-therapy should be given to prevent the seeding of mesothelioma cells down the needle track.

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